Coxsackie B-3 viruses cause myopericarditis in man and in inbred Balb/c mice. Following infection of the mice, virus localizes in the heart and other organs, replicates reaching peak titers on day 3 and decreasing to levels of no detectable infectious virus by day 7 to 14 when levels of cytolytic T cells in the spleen and virus neutralizing antibody in the serum peak. Myocarditis and necrosis are not evident in the heart before 5 days post infection, peak at 7 to 10 days, and depend upon functional T cells in the infected host, since T lymphocyte-deficient mice do not develop significant myocarditis. The proposed study will first attempt to identify the lymphoid cells present in inflammatory lesions in the Coxsackie B-3 Virus-infected Balb/c heart by histologic and immunoperoxidase staining and secondly, determine how T lymphocytes are involved in the myocarditis, either directly by specific T cell-mediated cytolysis of the myofibers, or indirectly by induction of IgG antibody to the virus or activation and chemotaxis of macrophages. The long term goal of the project is to more thoroughly understand the mechanisms of viral myocarditis and cardiac damage which could lead to new therapeutic treatments for the disease in humans.